[Fc receptor-dependent platelet activation results independently of glycoprotein complex IIb/IIIa].
Platelets of a patient with Glanzmann's thrombasthenia revealed the same activation pattern when stimulated with antibodies of patients with heparin-associated thrombocytopenia (HAT) or immune complexes. This was investigated by the 14C-serotonin release test and by changes in phosphorylation of p20 and p47. Platelet activation by HAT antibodies was completely inhibited by a moab against the platelet FcRII (IV. 3) and by Fc fragments of human IgG but not by F(ab)2 fragments. We conclude that platelet activation via the FcRII occurs independently of the glycoprotein complex IIb/IIIa. Therapeutical approaches targeting GP IIb/IIIa-fibrinogen interaction seem to be not appropriate in HAT.
Greinacher
A
A
Institut für Klinische Immunologie und Transfusionsmedizin, Justus-Liebig-Universität Giessen, Deutschland.
Liebenhoff
U
U
Kiefel
V
V
Presek
P
P
Mueller-Eckhardt
C
C
D001792:Blood Platelets / Q000276:immunology / Q000502:physiology*; D006493:Heparin; D006801:Humans; D010766:Phosphorylation; D015539:Platelet Activation; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000502:physiology*; D011961:Receptors, Fc / Q000502:physiology*; D012701:Serotonin / Q000097:blood; D013915:Thrombasthenia / Q000097:blood* / Q000276:immunology
D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D011961:Receptors, Fc; D012701:Serotonin; D006493:Heparin
Die Fc-Rezeptor-abhängige Thrombozytenaktivierung erfolgt unabhängig vom Glykoproteinkomplex IIb/IIIa.